Tamer Elkiran

Acute tumor lysis syndrome triggered by zoledronic Acid in a patient with metastatic lung adenocarcinoma.

We report the case of a 52-yr-old man with metastatic lung adenocarcinoma who developed tumor lysis syndrome after administration of zoledronic acid. Tumor lysis syndrome in solid tumors and the antitumor effect of the zolendronic acid are discussed in light of the pertinent literature.

Hepatotoxicity due to a possible interaction between cytosine arabinoside and dipyridamole: a case report

Cytosine arabinoside (ara-C) is a widely used antimetabolite chemotherapeutic drug. After being transported into the cytoplasm, ara-C is converted to 5-monophosphate nucleotide by deoxycytidine kinase. Ara-C is eliminated by deoxycytidine monophosphate deaminase and cytidine deaminase. Severe hepatic failure has been previously reported after the use of ara-C [2, 4], but the mechanism of this toxicity is not clear. Dipyridamole was reported to reduce the extracellular transport of ara-C by inhibiting nucleoside transporters, thereby increasing intracellular retention of ara-C [6, 7]. In the literature, there is no report describing a drug–drug interaction between dipyridamole and ara-C in humans. Here, we report a patient that developed multi-organ failure when treated with ara-C and dipyridamole concurrently.

A fortuitous episode of brachial plexopathy in a patient with metastatic breast cancer.

To the Editor, A 42-year-old lady, with a known diagnosis of metastatic breast cancer, was seen in the oncology ward for weakness in her left hand for the last 4 to 5 days. She described the episode as having emerged the morning after a long sleep on her left shoulder. Thereafter, she could only move her left upper limb with the aid of her right hand. The current medical history was otherwise noncontributory, and in fact, she was hospitalized for routine chemotherapy, but her complaint was only coincidental. Her previous history comprised right modified radical mastectomy (infiltrative ductal carcinoma, T2 N1 M0) in August 2000. Thereafter, on different occasions, she had received many combinations of chemotherapeutics including cyclophosphamide, doxorubicin, 5-fluorouracil, tamoxifen, docetaxel, letrozole, vinorelbine, mitomycin C, ifosfamide, etoposide, and radiotherapy to the operation site and the right axilla. She had also had previous lung and liver metastases. The physical examination was consistent with moderatesevere motor function loss in the left upper extremity: biceps (4/5), triceps (3/5), wrist extensors (2/5), wrist flexors (3/5), finger abductors and adductors (2/5), and thumb opposition (2/5) with hypoesthesia. Unexpectedly, the deep tendon reflexes (DTR) were slightly increased with accompanying Hoffmans reflex positivity. No mass in the axilla or its nearby could be palpated. The neurologic examination of the right upper extremity and the lower extremities was unremarkable. The patient was clinically diagnosed as having left-sided compressive brachial plexopathy (BP), and an electromyography (EMG) was planned. Cranial magnetic resonance imaging (MRI) was also performed to substantiate our findings of increased DTR and Hoffmans positivity. The MRI revealed multiple intracranial metastases (Fig. 1). The patients treatment was then switched onto capecitabine, dexamethasone, and cranial radiotherapy. A rehabilitation protocol for her BP, consisting of electrical stimulation and strengthening exercises, was commenced. Fortunately, our patient responded rapidly and became significantly better even at the time of EMG. Electrophysiologic evaluations yielded a regenerating type of BP lesion without any findings of denervation, conduction block, or myokymia, whereby C8 through T1 involvement was predominant. After 2 weeks of physiotherapy, as the strength of the aforementioned muscle groups improved quite well (4-5/5), she was discharged to complete her rehabilitation program with home exercises and was called for a control visit for her breast cancer. Brachial plexus syndromes in patients with breast cancer ensue because of various mechanisms including metastatic involvement, radiation injury, soft tissue changes due to surgery or radiation, ischemia, idiopathic causes, or any combination of these [1,2]. Clinical history, neurologic examination, EMG, and imaging studies aid in the differential diagnosis and also in the management. Herewith, our patients BP displayed 2 extraordinary findings; it was on the contralateral side of the malignancy, and there were concomitant upper motor neuron findings (increased DTR and Hoffmans positivity). In this regard, we would like to emphasize the role of prompt neurologic examination during the follow-up of these patients. In our case, it heralded the central nervous system involvement, and the patients chemotherapy was tailored accordingly. Last but not least, keeping in mind the increased susceptibility of the peripheric nerves of these patients receiving many drugs with potential neurotoxicity, we believe that physicians should always be vigilant against unexpected and otherwise challenging neurologic scenarios.